Cell Mol Neurobiol. 2015 Oct ;35(7):943-52. Epub 2015 Apr 14. PMID: 25869596
Ginkgolide B Protects Neurons from Ischemic Harm by Inhibiting the Expression of RTP801.
RTP801 (often known as REDD1), a stress-related protein, is induced by a number of environmental stresses resembling ischemia and cigarette smoke. Though ischemia can dramatically up-regulate RTP801 expression in mind ischemia, to date, the precise relation between RTP801 and neuronal dying in ischemia is poorly understood. Within the present research, utilizing oxygen and glucose deprivation as an in vitro ischemic mannequin in main cultured cortical neurons, we discovered that the expression of RTP801 elevated progressively with prolongation of ischemic length, through which the expression of RTP801 is positively correlated with the discharge of lactate dehydrogenase (LDH) in neurons, and knockdown of RTP801 promoted neuronal survival in ischemia-reperfusion. It was additional discovered that ginkgolide B (GB) might considerably enhance cell viability and reduce LDH launch, and on the similar time cut back the degrees of RTP801 mRNA and protein in neurons after ischemia and reperfusion. Furthermore, GB-induced discount in expression of RTP801 was blocked by software of LY294002, a particular inhibitor of phosphatidylinositol 3-kinase (PI3K). These outcomes reveal that RTP801 might play a detrimental position on neurons in ischemia, and GB may defend neurons in opposition to ischemic damage by inhibiting RTP801 expression through PI3K pathway.